Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Mechanisms of Microbial Disease > Chapter 17 > Flashcards

Chapter 17 Flashcards

1
Q

What is a true food poisoning?

A

Ingestion of a pre-formed toxin (no organism needed)
Faster acting (hours)
Survive cooking/heating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a food-associated infection?

A

Food is a vehicle for a pathogen

Slower onset of symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can a pathogen change fluid balance to cause GI disease?

A

Change the balance of water and electrolytes in the small bowel causing massive fluid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do cell destruction and inflammation occur to cause GI disease?

A

Invasion and/or cytotoxin production

Will lead to a fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does invasion cause GI disease?

A

Penetrates intestinal mucosa allowing the pathogen to spread and multiply outside of the bowel
Blood or pus found in feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is diarrhea?

A

The most common outcome of GI tract infections that increases fluid and electrolyte loss in the gut lumen (unformed or liquid faeces)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does diarrhea allow?

A

Allows the host to get rid of the pathogen and the pathogen to disseminate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does diarrhea differ in resource-rich and resource poor region?

A

Poor: Major cause of mortality in children
Rich: Usually mild and self-limiting except in very young, elderly and immunocompromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do we determine the cause of the diarrhea?

A

Generally difficult to identify based solely on symptoms (important in outbreaks)
Get patient history (food intake, travel)
Macroscopic and microscopic examination of feces for blood and pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a common bacterial cause of diarrhea?

A

E. coli, most versatile, member of gut flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does Enteropathogenic E. coli (EPEC) cause?

A

Sporadic cases and outbreak of diarrhea in babies and young children
No toxin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the virulence factors of EPEC?

A

Adhesions, bundle-forming pili and intimin to attach to epithelial cells and microvillus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does Enterotoxigenic E. coli (ETEC) cause?

A

Most important cause of bacterial diarrhea in children

Presence of E. coli not necessarily important, plasmid is (Need lots to cause problems)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does ETEC work?

A

Binds to receptors on the cell membrane of the small intestine and produces plasma encoded toxins (heat labile and stable)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do the 2 plasmid encoded toxins of ETEC work?

A 
Heat labile (LT) toxin increases cAMP, similar mode of action to cholera
Heat stable (ST) toxin increases guanylate cyclase activity which increase cGMP and fluid secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is Enterohaemorrhagic E.coli (EHEC) found?

A

In the intestine of healthy cattle (uncooked ground beef, unpasteurized milk/juices, contaminated water, bean sprouts, celery)
“Hamburger disease”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does EHEC work?

A

Invasive and makes toxins that damage the large intestine by inhibiting protein synthesis
Verotoxin I and II (VTEC) or “Shiga like toxin” (SLT-1 and SLT-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some symptoms of EHEC?

A

Ulceration and bleeding of the large intestine causing bloody diarrhea
Destruction of RBC cause anemia (fatigue, weakness)
Low platelet count and sudden kidney damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the ID50 of EHEC?

A

Very small, only takes a few to cause problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the serotype of EHEC?

A

Serotype O157:H7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some complications of EHEC?

A 
Hemorrhagic colitis (destruction of mucosa leading to hemorrhage and bloody diarrhea)
Hemolytic ureic syndrome (HUS-toxin in blood stream)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What may account for the kidney damage by EHEC?

A

Verotoxin receptors found on the renal epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does Enteroinvasive E. coli (EIEC) work?

A

Attach to the mucosa of the large intestine, invade the cells via endocytosis, multiply, spread to adjacent cells and cause tissue destruction, inflammation and ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the symptoms of EIEC?

A

Blood and mucous in the stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does enteroaggregative E. coli (EAEC) work?

A

Aggregation using plasmid-encoded fimbria

Toxins produced but role uncertain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does EAEC appear on tissue culture cells?

A

Like stacked bricks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does Diffuse-aggregative E.coli (DAEC) produce?

A

alpha-hemolysin and cytotoxic necrotizing factor

Role in diarrhea not well understood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How do we ID EHEC strain?

A

By probing for shiga toxin genes or proteins (use antibodies-ELISA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do we ID EIEC strain?

A

Look for the invasion of tissue culture cells or the presence of invasion associated genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do we treat diarrhea?

A

No antibiotics as this can cause more toxin to be released

Fluid and electrolyte replacement and prevention (clean water, pasteurization, proper cooking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why are antidiarrheal medications (immodium) bad?

A

Desensitizes the intestinal epithelium to the toxin, increasing the contact time with the intestinal wall which can increase disease severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How do we treat HUS?

A

Urgent treatment with dialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does Salmonella spp cause?

A

Gastroenteritis, food poisoning and enteric fever (S. typhi makes typhoid fever)

34
Q

Where does salmonella spp. come from?

A

Meat, poultry, eggs, dairy products, farmed fishes

Cross contamination with animals, food and humans, water

35
Q

What are the symptoms of salmonella spp. infection?

A

6-48 hours after ingestion nausea, vomiting and diarrhea occur, usually self-limiting

36
Q

What must be done with food handlers when they have a salmonella spp. infection?

A

Excluded from work until 3 fecal specimens are negative

May be excreted in feces for several weeks post infection

37
Q

What are the symptoms of enteric fever?

A

Initial: Headache, fever, abdominal tenderness, constipation

Diarrheal stage: Gallbladder and Peyer’s patches

38
Q

How does salmonellosis colonize in the body?

A

Hides in a vacuole in the host cell, divides, then hides in monocytes to travel in blood stream and cause systemic infection
Chronic colonization

39
Q

How do we diagnose salmonellosis?

A

Recover from blood and stools

40
Q

Where does salmonellosis colonize chronically?

A

In the gallbladder and biliary tree with no symptoms but still constantly shedding (Typhoid Mary)

41
Q

What is the most common cause of bacterial gastroenteritis?

A

Campylobacter
High ID50
Heat sensitive, invasive

42
Q

What are the symptoms of campylobacter infection?

A

Lasts 2-5 days
Diarrhea with blood and pus, painful (2-3 days)
Abdominal pain lasting longer
Self-limiting

43
Q

Where does campylobacter come from?

A

Poultry, contaminated meat, water and unpasteurized milk

44
Q

How is campylobacter identified?

A

By the S-shaped cells under the microscope

45
Q

How is campylobacter treated?

A

Using fluoroquinolone and macrolides

46
Q

What does vibrio cause?

A

Cholera (rapid dehydration by rice water stools), only infects humans

47
Q

Where is vibrio in endemic?

A

Southeast Asia, parts of south america and africa

48
Q

Where does vibrio come from?

A

Water environments, fish, shellfish

49
Q

What are rice water stools?

A

Stools free of RBCs and WBCs, pretty much just water

Diagnostic tool

50
Q

What is the pathogenesis of vibrio?

A

Mostly due to toxins that it only produces in the human gut (AB subunit, activating adenylate cyclase)

51
Q

What is vibrio sensitive to?

A

Stomach acid, need very very high number of cells to get sick

52
Q

What are the subsets of Shigella spp.?

A

S. sonnet (mild, most common in Canada)
S. flexneri
S. dysenteriae (most serious)
S. boydii

53
Q

What is the ID50 of shigellosis?

A

Very low (

54
Q

What toxins does shigella spp. produce?

A 
Shiga toxin (similar to E.coli 0157)
Cytotoxic, enterotoxin, nerotoxic
55
Q

What is the pathogenesis of shigella spp.?

A

Enters an epithelial cell of the intestinal tract, multiplies inside, invades neighbouring cells. When released, epithelial cell is killed, forming an access
Kind of like salmonella

56
Q

What is a complication of shigellosis?

A

Damage to the epithelial and kidney cells causing HUS

57
Q

How can shigellosis be treated?

A

Mild is treated by rehydration

Severe needs antibiotics

58
Q

What is clostridium difficile?

A

A broad spectrum antibiotic-associated diarrhea (antibiotic resistant, when other microflora are killed, it takes over)
Most common cause of hospital acquired diarrhea
Spore formers, toxins

59
Q

What does clostridium difficile cause?

A

Mild-watery diarrhea to life-threatening toxic megacolon (surgical intervention)
Pseudomembranes forming pseudomembranous colitis (fibrin, neutrophils, mucin, cellular debris)

60
Q

What toxins does clostridium difficile produce?

A

Ted A (toxin A) and Ted B (toxin B) encoded by pathogenicity locus on chromosome together with negative and positive regulators of their expression

61
Q

What is the emergent strain of clostridium difficile?

A

C.difficile 027 produces more TedA and B due to deletion in regulatory gene (tcdC) that down regulates the production of two toxins

62
Q

How is clostridium difficile treated?

A 
Antibiotics for a serious infection
Fecal transplant (successful, rejection rate due to genetic and gender link, need someone who hasn't been on antibiotics in 5 years, stomach acid is a problem)
63
Q

Does clostridium difficile ever go away?

A

Infection persists forever, most people never get their normal microflora back

64
Q

What are some common causative agents for food poisoning?

A

Staph aureus enterotoxin (8 types, heat stable, enzyme resistant), clostridium botulinum toxin

65
Q

How do S. aureus enterotoxins work?

A 
It is a super antigen that binds to MHC class II molecules and cause T-cell stimulation
Body's reaction is much more aggressive
66
Q

What are the side effects of S. aureus enterotoxins?

A

Affects CNS, severe vomiting 3-6 hours after consumption, no diarrhea, complete recovery in 24 hours

67
Q

Where is listeria monocytogenes found?

A

Animals, the environment, undercooked food, unpasteurized food, soft cheese

68
Q

Who has an enhanced risk for listeriosis?

A

Pregnant women (can cross placenta) and immunocompromised individuals

69
Q

What is the ID50 of listeria monocytogenes?

A
70
Q

Is listeria monocytogenes susceptible to heat?

A

Yes, but survives and grows very well at room temperature (multiplies at 4 degrees)

71
Q

How does the virulence of listeria monocytogenes work?

A

Gets inside cells via endocytosis, forms actin tail and spreads from cell to cell via endocytosis without ever leaving host cells
Survives on macrophages

72
Q

What are the most common cause of gastroenteritis and diarrhea?

A

Viruses (rotavirus, norovirus), specific to human

Impact nutritional status and growth if contracted at young age

73
Q

What are rotaviruses?

A

Lt wheel naked viruses spread by oral-decal transmission

74
Q

What are the symptoms of rotavirus infection?

A

Vomiting, diarrhea (very high numbers-contagious), fever

Only 6-7 days

75
Q

How is rotavirus infection treated?

A

Fluid and salt replacement

Use clean, uncontaminated water

76
Q

How can rotavirus be prevented?

A

Using a vaccination

77
Q

What is a norovirus? Where does it commonly cause infection?

A

Calcivirus family, most common cause of food illness outbreaks
Schools, nursing homes, families, cruise ships

78
Q

What is the incubation period and rate of infection for norovirus?

A

24-48 hours

50% rate of infection (highly infectious)

79
Q

How can we determine if it is norovirus?

A

Unculturable so use an electron microscope or RT-PCR

80
Q

What is the 2nd largest cause of mortality and morbidity in the world?

A

GI tract infections

Mechanisms of Microbial Disease (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions